Helicobacter pylori inflammation and immunity

Abstract

Gastric inflammation is a significant contributor to the disease process associated with Helicobacter pylori infection. It appears that both bacterial genes and differential host responses make interrelated contributions to gastritis and disease outcome after H. pylori infection. While the cag pathogenicity island (PAI) continues to be a focus for much of this investigation on the bacterial side, other bacterial genes/proteins are certainly important as well. On the host cell side, significant progress is being made defining the eucaryotic signaling cascades induced after host cells interact with H. pylori. The role of host cell cytokines, gastric acid, and mast cells is also being actively studied. Prospects for control of H. pylori associated disease continue to include vaccination. The mechanism(s) for vaccine-mediated control of H. pylori infection and disease remain ill-defined but recent evidence from animal models suggests that the inflammatory response may be involved. Manipulating the host response to H. pylori infection in humans to take advantage of the possible beneficial effects of inflammation, while minimizing its detrimental effects is a significant challenge for the future.

Therapeutic Vaccination againstHelicobacter pyloriin the Beagle Dog Experimental Model: Safety, Immunogenicity, and Efficacy

“…Particularly in the study 1 (weekly vaccination), the reduction of gastritis was a slow process, requiring several weeks to be achieved. This effect can also be explained with the observation, made in several vaccination studies, that a protective local immune reaction against H. pylori can produce per se a transient gastric inflammation (25). Thus, within a short time after vaccination, it is not possible to distinguish a "protective" inflammation from that induced by H. pylori.…”

Impact of CagA Status on Serum Gastrin and Pepsinogen I and II Concentrations in Japanese Children withHelicobacter PyloriInfection

“…4 One virulent factor that has been identified is cytotoxin-associated gene product (CagA), which is encoded by the cagA gene. 5 CagA status is associated with a higher risk of peptic ulcers or gastric cancers in Western countries, 4,5 but not in Japanese adults. 4,6,7 There is little information, however, on CagA seroprevalence in Japanese children.…”

B-Cell and T-Cell Immune Responses to ExperimentalHelicobacter pyloriInfection in Humans

“…The histological characteristics of the mucosal inflammation contain features of both acute and chronic inflammation. Although much is known about the clinical manifestations of chronic H. pylori infection, there is little information regarding the immune response in the early phases of infection (11,39). One major obstacle to the study of the early events in H. pylori infection in humans has been the difficulty in determining when an individual actually becomes infected.…”